Despite recent advances in cancer research, the development of cancer cell-specific therapies has remained elusive. This “targeted approach” should ideally reduce the side effects due to the toxicity towards normal cells, while increasing the specificity to the cancer cells. There are a limited number of targeted cancer therapies. For example, antisense therapy works at the molecular level to stop the process by which cancer-causing proteins are produced by host tumor cells. Gene therapy involves development of delivery systems to deliver a therapeutic gene into cancer cells. These molecular treatments theoretically will result in (i) increased sensitivity of cancer cells to a specific drug; (ii) replacement of damaged genes that cause tumorigenesis, metastasis, and angiogenesis; (iii) enhanced immune detection. To date, therapies actually providing such benefits using gene therapy have not been achieved.
Chemotherapy is the traditional approach to cancer treatment. Advances in biotechnology have promoted the development of better (e.g., targeted) drugs with fewer side effects. While promising, these molecular biology-based therapies require complex delivery systems, and protocols that are both difficult to practice and are excessively costly. The further improvement of cancer treatments requires a better understanding of the components that make up cancer cells.
All cells have surface receptors that work in concert with associated proteins to signal and cause host cell activities. For example, the epidermal growth factor receptor helps control cell growth, repair and metastasis. Many tumor cells have been found to have higher numbers of epidermal growth factor receptors than normal cells. Cetuximab (IMC-225) was specifically designed to target and block epidermal growth factor receptors preventing cell division and repair during rapid growth.
Unfortunately, not all carcinomas have high numbers of epidermal growth factor receptors. Other targeted therapies have presented similar problems. Recently, the FDA approved the first targeted cancer therapy drug, Herceptin (trastuzumab), a monoclonal antibody used to treat metastatic breast cancer. By blocking a protein called HER-2, cancer cell growth was stopped. HER-2 is a factor in about 25 to 30 percent of breast cancers. While other targeted cancer therapies are being developed, there will certainly not be one target, nor one therapy that stops or kills all tumors. Consequently, the development of therapies to exploit newly identified specific targets associated with tumor proliferation will be required.
The cloning of the retroviral nef genes has been taught and some functions (but not anti-carcinoma properties) have been taught in U.S. Pat. No. 6,020,171 of Saito, et al, issued Feb. 1, 2000, which is incorporated herein by reference in its entirety.